Direct stimulation of BAT thermogenesis does not affect hypothalamic neuropeptide Y

被引:5
作者
Bing, C
Hopkins, D
Wang, Q
Frankish, H
Buckingham, R
Williams, G [1 ]
机构
[1] Univ Liverpool, Dept Med, Diabet & Endocrinol Res Unit, Liverpool L69 3GA, Merseyside, England
[2] SmithKline Beecham Pharmaceut, Welwyn Garden City AL6 9AR, Herts, England
基金
英国惠康基金;
关键词
beta(3)-adrenoceptor agonist; BRL; 35135; brown adipose tissue; thermogenesis; NPY; hypothalamus; rat;
D O I
10.1016/S0196-9781(97)00272-6
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Acute cold exposure which significantly stimulated thermogenesis in brown adipose tissue (BAT), also increased neuropeptide Y (NPY) levels in its hypothalamic sites of release without affecting NPY synthesis, suggesting that NPY release is acutely inhibited. To clarify whether these changes in NPY are the cause or consequence of BAT activation, we studied whether hypothalamic NPY and NPY mRNA levels in rats were affected by acute intraperitoneal injection of the beta(3)-adrenoceptor agonist BRL 35135 (500 mu g/kg), which directly activates BAT thermogenesis. BRL. 35135 treatment doubled BAT uncoupling protein mRNA levels (p < 0.05), and increased core temperature by 0.4 degrees C (p < 0.05), but neither hypothalamic regional NPY levels nor hypothalamic NPY mRNA levels were affected by BRL 35135. This suggests that the NPY changes induced by cold exposure are not the result of BAT activation, and is consistent with the hypothesis that decreased NPY release during cold exposure might disinhibit the sympathetic innervation that drives BAT thermogenesis. (C) 1998 Elsevier Science Inc.
引用
收藏
页码:167 / 170
页数:4
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